Family or personal history. Your risk increases if you have prediabetes — a precursor to type 2 diabetes — or if a close family member, such as a parent or sibling, has type 2 diabetes. You're also at greater risk if you had gestational diabetes during a previous pregnancy, if you delivered a very large baby or if you had an unexplained stillbirth.
The patient, physician, nurse, and dietician must carefully evaluate the patient's life style, nutritional needs, and ability to comply with the proposed dietary prescription. There are a variety of meal planning systems that can be used by the patient with diabetes; each has benefits and drawbacks that need to be evaluated in order to maximize compliance. Two of the most frequently used ones are the exchange system (see accompanying table) and the carbohydrate counting system.

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At the same time that the body is trying to get rid of glucose from the blood, the cells are starving for glucose and sending signals to the body to eat more food, thus making patients extremely hungry. To provide energy for the starving cells, the body also tries to convert fats and proteins to glucose. The breakdown of fats and proteins for energy causes acid compounds called ketones to form in the blood. Ketones also will be excreted in the urine. As ketones build up in the blood, a condition called ketoacidosis can occur. This condition can be life threatening if left untreated, leading to coma and death.

Oral diabetes medications may also come in combination tablets such as Metaglip (glipizide/metformin), Prandimet (repaglinide/metformin), Glucovance (glyburide/metformin), Janumet (sitagliptin/metformin), Avandamet (rosiglitazone/metformin), Avandaryl (rosiglitazone/ glimepiride), Duetact (pioglitazone/glimepiride), Actoplus Met (pioglitazone/metformin).

In the exchange system, foods are divided into six food groups (starch, meat, vegetable, fruit, milk, and fat) and the patient is taught to select items from each food group as ordered. Items in each group may be exchanged for each other in specified portions. The patient should avoid concentrated sweets and should increase fiber in the diet. Special dietetic foods are not necessary. Patient teaching should emphasize that a diabetic diet is a healthy diet that all members of the family can follow.

Insulin is released into the blood by beta cells (β-cells), found in the islets of Langerhans in the pancreas, in response to rising levels of blood glucose, typically after eating. Insulin is used by about two-thirds of the body's cells to absorb glucose from the blood for use as fuel, for conversion to other needed molecules, or for storage. Lower glucose levels result in decreased insulin release from the beta cells and in the breakdown of glycogen to glucose. This process is mainly controlled by the hormone glucagon, which acts in the opposite manner to insulin.[63]
Although age of onset and length of the disease process are related to the frequency with which vascular, renal, and neurologic complications develop, there are some patients who remain relatively free of sequelae even into the later years of their lives. Because diabetes mellitus is not a single disease but rather a complex constellation of syndromes, each patient has a unique response to the disease process.

FASTING GLUCOSE TEST. Blood is drawn from a vein in the patient's arm after a period at least eight hours when the patient has not eaten, usually in the morning before breakfast. The red blood cells are separated from the sample and the amount of glucose is measured in the remaining plasma. A plasma level of 7.8 mmol/L (200 mg/L) or greater can indicate diabetes. The fasting glucose test is usually repeated on another day to confirm the results.


An organ in the abdomen called the pancreas produces a hormone called insulin, which is essential to helping glucose get into the body's cells. In a person without diabetes, the pancreas produces more insulin whenever blood levels of glucose rise (for example, after a meal), and the insulin signals the body's cells to take in the glucose. In diabetes, either the pancreas's ability to produce insulin or the cells' response to insulin is altered.
gestational diabetes diabetes mellitus with onset or first recognition during pregnancy, usually during the second or third trimester. In some cases mild, undetected glucose intolerance was present before pregnancy. It often disappears after the end of the pregnancy, but many women with this condition develop permanent diabetes mellitus in later life. Although the disordered carbohydrate metabolism is usually mild, prompt detection and treatment are necessary to avoid fetal and neonatal morbidity and mortality.
Type 1 diabetes is partly inherited, with multiple genes, including certain HLA genotypes, known to influence the risk of diabetes. In genetically susceptible people, the onset of diabetes can be triggered by one or more environmental factors,[42] such as a viral infection or diet. Several viruses have been implicated, but to date there is no stringent evidence to support this hypothesis in humans.[42][43] Among dietary factors, data suggest that gliadin (a protein present in gluten) may play a role in the development of type 1 diabetes, but the mechanism is not fully understood.[44][45]
DM affects at least 16 million U.S. residents, ranks seventh as a cause of death in the United States, and costs the national economy over $100 billion yearly. The striking increase in the prevalence of DM in the U.S. during recent years has been linked to a rise in the prevalence of obesity. About 95% of those with DM have Type 2, in which the pancreatic beta cells retain some insulin-producing potential, and the rest have Type 1, in which exogenous insulin is required for long-term survival. In Type 1 DM, which typically causes symptoms before age 25, an autoimmune process is responsible for beta cell destruction. Type 2 DM is characterized by insulin resistance in peripheral tissues as well as a defect in insulin secretion by beta cells. Insulin regulates carbohydrate metabolism by mediating the rapid transport of glucose and amino acids from the circulation into muscle and other tissue cells, by promoting the storage of glucose in liver cells as glycogen, and by inhibiting gluconeogenesis. The normal stimulus for the release of insulin from the pancreas is a rise in the concentration of glucose in circulating blood, which typically occurs within a few minutes after a meal. When such a rise elicits an appropriate insulin response, so that the blood level of glucose falls again as it is taken into cells, glucose tolerance is said to be normal. The central fact in DM is an impairment of glucose tolerance of such a degree as to threaten or impair health. Long recognized as an independent risk factor for cardiovascular disease, DM is often associated with other risk factors, including disorders of lipid metabolism (elevation of very-low-density lipoprotein cholesterol and triglycerides and depression of high-density lipoprotein cholesterol), obesity, hypertension, and impairment of renal function. Sustained elevation of serum glucose and triglycerides aggravates the biochemical defect inherent in DM by impairing insulin secretion, insulin-mediated glucose uptake by cells, and hepatic regulation of glucose output. Long-term consequences of the diabetic state include macrovascular complications (premature or accelerated atherosclerosis with resulting coronary, cerebral, and peripheral vascular insufficiency) and microvascular complications (retinopathy, nephropathy, and neuropathy). It is estimated that half those with DM already have some complications when the diagnosis is made. The American Diabetes Association (ADA) recommends screening for DM for people with risk factors such as obesity, age 45 years or older, family history of DM, or history of gestational diabetes. If screening yields normal results, it should be repeated every 3 years. The diagnosis of DM depends on measurement of plasma glucose concentration. The diagnosis is confirmed when any two measurements of plasma glucose performed on different days yield levels at or above established thresholds: in the fasting state, 126 mg/dL (7 mmol/L); 2 hours postprandially (after a 75-g oral glucose load) or at random, 200 mg/dL (11.1 mmol/L). A fasting plasma glucose of 100-125 mg/dL (5.5-6.9 mmol/L) or a 2-hour postprandial glucose of 140-199 mg/dL (7.8-11 mmol/L) is defined as impaired glucose tolerance. People with impaired glucose tolerance are at higher risk of developing DM within 10 years. For such people, lifestyle modification such as weight reduction and exercise may prevent or postpone the onset of frank DM. Current recommendations for the management of DM emphasize education and individualization of therapy. Controlled studies have shown that rigorous maintenance of plasma glucose levels as near to normal as possible at all times substantially reduces the incidence and severity of long-term complications, particularly microvascular complications. Such control involves limitation of dietary carbohydrate and saturated fat; monitoring of blood glucose, including self-testing by the patient and periodic determination of glycosylated hemoglobin; and administration of insulin (particularly in Type 1 DM), drugs that stimulate endogenous insulin production (in Type 2 DM), or both. The ADA recommends inclusion of healthful carbohydrate-containing foods such as whole grains, fruits, vegetables, and low-fat milk in a diabetic diet. Restriction of dietary fat to less than 10% of total calories is recommended for people with diabetes, as for the general population. Further restriction may be appropriate for those with heart disease or elevated cholesterol or triglyceride levels. The ADA advises that high-protein, low-carbohydrate diets have no particular merit in long-term weight control or in maintenance of a normal plasma glucose level in DM. Pharmaceutical agents developed during the 1990s improve control of DM by enhancing responsiveness of cells to insulin, counteracting insulin resistance, and reducing postprandial carbohydrate absorption. Tailor-made insulin analogues produced by recombinant DNA technology (for example, lispro, aspart, and glargine insulins) have broadened the range of pharmacologic properties and treatment options available. Their use improves both short-term and long-term control of plasma glucose and is associated with fewer episodes of hypoglycemia. SEE ALSO insulin resistance

Type 1 diabetes can occur at any age, and a significant proportion is diagnosed during adulthood. Latent autoimmune diabetes of adults (LADA) is the diagnostic term applied when type 1 diabetes develops in adults; it has a slower onset than the same condition in children. Given this difference, some use the unofficial term "type 1.5 diabetes" for this condition. Adults with LADA are frequently initially misdiagnosed as having type 2 diabetes, based on age rather than cause[46]
Type 2 diabetes begins with insulin resistance, a condition in which cells fail to respond to insulin properly.[2] As the disease progresses, a lack of insulin may also develop.[12] This form was previously referred to as "non insulin-dependent diabetes mellitus" (NIDDM) or "adult-onset diabetes".[2] The most common cause is a combination of excessive body weight and insufficient exercise.[2]
At the same time that the body is trying to get rid of glucose from the blood, the cells are starving for glucose and sending signals to the body to eat more food, thus making patients extremely hungry. To provide energy for the starving cells, the body also tries to convert fats and proteins to glucose. The breakdown of fats and proteins for energy causes acid compounds called ketones to form in the blood. Ketones also will be excreted in the urine. As ketones build up in the blood, a condition called ketoacidosis can occur. This condition can be life threatening if left untreated, leading to coma and death.
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